wound-healing-reading-chapters
wound-healing-reading-chapters
wound-healing-reading-chapters
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SRPS Volume 10, Number 7, Part 1<br />
cell to radiation damage is directly proportional to<br />
its mitotic rate. The most sensitive cells are those<br />
which divide rapidly, such as cells of the skin, bone<br />
marrow, and gastrointestinal tract. In addition to<br />
sensitivity of the exposed cell, morbidity from<br />
radiation depends on the dose received, time over<br />
which the dose is received, volume of tissue irradiated,<br />
and type of radiation. 399 Cellular changes<br />
resulting from low-dose radiation are probably due<br />
to an apoptotic mechanism, whereas changes<br />
related to high-dose radiation are probably due to<br />
direct cellular necrosis.<br />
The direct effects of radiation can be immediate,<br />
acute (days to weeks), or delayed (months to<br />
years). Acute effects result from necrosis of the rapidly<br />
proliferating cell lines. A transient, faint erythema<br />
may appear during the first week of treatment due<br />
to dilation of capillaries and may be associated with<br />
an increase in vascular permeability. Radiation<br />
inhibits mitotic activity in the germinal cells of the<br />
epidermis, hair follicles, and sebaceous glands. Epilation<br />
and dryness of the skin occur. By the third or<br />
fourth week of radiation, typical erythema is localized<br />
to the radiation field and the skin is noticeably<br />
red, edematous, warm, and tender. Larger vessels<br />
may be obstructed by fibrin thrombi, edema is<br />
prominent, and there may be small foci of hemorrhage.<br />
400 Cellular exudate is rare. If the total radiation<br />
dose to the skin does not exceed 30Gy, the<br />
erythema phase is followed during the fourth or<br />
fifth week by a dry desquamation phase characterized<br />
by pruritus, scaling, and an increase in melanin<br />
pigmentation in the basal layer. Within 2 months<br />
the inflammatory exudate and edema have subsided,<br />
leaving an area of brown pigmentation.<br />
If the total radiation dose to the skin is >40Gy,<br />
the erythema phase is followed by a moist desquamation<br />
phase. This stage usually begins in the fourth<br />
week and is often accompanied by considerable<br />
discomfort. Bullous formation occurs above the basal<br />
layer and sometimes just below the epidermis. Eventually<br />
the roofs of the bullae are shed and the entire<br />
epidermis may be lost in portions of the irradiated<br />
area. Edema and fibrinous exudate persist. In the<br />
absence of infection, reepithelization of the<br />
denuded skin usually begins within 10 days. Ulcers<br />
may appear 2 weeks or more after radiation exposure.<br />
These ulcers are a result of direct necrosis of<br />
the epidermis; they usually heal but tend to<br />
recur. 399,401<br />
Approximately 1 year after radiation treatment<br />
the epidermis is thin, dry, and semitranslucent, with<br />
vessels easily seen. Hair follicles and sebaceous<br />
glands are usually absent. Some sweat glands may<br />
also have been destroyed. In time, increasing fibrosis<br />
of the skin is present. Much of the collagen and<br />
subcutaneous adipose tissue are replaced by atypical<br />
fibroblasts and dense fibrous tissue that may<br />
cause induration of the skin and may limit movement.<br />
In radiation injury of soft tissue, fibrinous<br />
exudate accumulates under the epidermis. Characteristic<br />
features of delayed radiation lesions are<br />
eccentric myointimal proliferation of the small<br />
arteries and arterioles as well as telangiectasia. These<br />
changes may progress to thrombosis or complete<br />
obstruction. Delayed ulcers are more common than<br />
acute ulcers and result from ischemic changes in<br />
small arteries and arterioles; they heal slowly and<br />
may persist for several years. Irradiated skin in the<br />
chronic stage is thin, hypovascularized, extremely<br />
painful, and easily injured by any slight trauma or<br />
infection. 399,401<br />
Skin reactions to radiation should be treated early<br />
to prevent complications later. Keeping the skin<br />
moist and pliable to prevent fissures and cracks and<br />
free of infection is extremely important. Mendelsohn<br />
et al 402 has compiled a list of products to treat<br />
radiation-induced skin changes (Table 10). If an<br />
ulcer develops, the normal <strong>wound</strong> care protocols<br />
should be initiated. In severe cases, wide<br />
debridement and a skin graft or flap coverage may<br />
be necessary.<br />
Treatment with hyperbaric oxygen accelerates<br />
<strong>healing</strong> in some patients, 403,404 but its effectiveness<br />
in soft-tissue necrosis from radiation injury is<br />
unproven. Experimental therapies include topical<br />
TGF-β1, 405 granulocyte-macrophage colonystimulating<br />
factor (GM-CSF), 406 orgotein (a Cu/Zn<br />
chelate with superoxide dismutase), 407 topical vitamin<br />
C, 408,409 topical corticosteroids, 410 glucorticoids,<br />
411 NSAIDs, 412 aloe vera gel, 413,414 heliumneon<br />
laser treatments, 415 and oral pentoxifylline<br />
treatment. 416<br />
HIGH-PRESSURE INJECTION INJURIES<br />
High-pressure injection devices such as are used<br />
for painting, cleaning, degreasing, etc. can produce<br />
pressures of 600–12,000psi. 417,418 The substance<br />
enters the skin through a seemingly insignificant<br />
35